Regular ArticlesEffects of Na+/Ca2+-exchanger Overexpression on Excitation–contraction Coupling in Adult Rabbit Ventricular Myocytes
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2021, Epigenetics in Cardiovascular DiseaseNew experimental evidence for mechanism of arrhythmogenic membrane potential alternans based on balance of electrogenic I<inf>NCX</inf>/I <inf>Ca</inf> currents
2012, Heart RhythmCitation Excerpt :INCX predominance was achieved by in vivo NCX gene transfer by using a modified cross-clamping method.9 Western blot from in vitro NCX overexpression showed that NCX protein expression was indeed increased by (3.8 ± 2.9)-fold compared with control (n = 3), and previously Ranu et al10 demonstrated that the overexpression of NCX increases INCX, with no change in ICa. ICa predominance was achieved by INCX inhibition or ICa enhancement.
Systematic characterization of the ionic basis of rabbit cellular electrophysiology using two ventricular models
2011, Progress in Biophysics and Molecular BiologyCitation Excerpt :Many experimental results support the primary role of GCaL, GNaK and GNaCa on systolic [Ca2+]i shown in our simulations. The important role played by GNaK in modulating systolic [Ca2+]i levels in both rabbit models is supported by the marked increase in cell force of contraction and calcium levels caused by INaK inhibitors, such as ouabain (Giles and Shimoni, 1989; Kodama et al., 1981; McCans et al., 1974; Schillinger et al., 2003) and strophantidine (Loughrey et al., 2003; Ranu et al., 2002; Szigligeti et al., 1996). Furthermore, experimental results showing reduction of cell contraction (related to systolic [Ca2+]i) caused by the ICaL blocker verapamil (Mahajan et al., 2008a), are consistent with the importance of GCaL in determining systolic [Ca2+]i levels.
Targeted GLUT-4 deficiency in the heart induces cardiomyocyte hypertrophy and impaired contractility linked with Ca<sup>2+</sup> and proton flux dysregulation
2010, Journal of Molecular and Cellular Cardiologyβ-Adrenergic receptor stimulated Ncx1 upregulation is mediated via a CaMKII/AP-1 signaling pathway in adult cardiomyocytes
2010, Journal of Molecular and Cellular CardiologyCitation Excerpt :Transgenic overexpression of the cytosolic splice variant, CaMKIIδc, induces severe heart failure associated with SR Ca2+ leak and reduced SR Ca2+ content [57]. Correspondingly, the upregulation of Ncx1 contributes directly to limiting SR loading, contractile dysfunction and greater potential for delayed after depolarizations, which lead to ventricular tachycardia [9,18–20]. Furthermore, numerous studies of human and animal models of heart failure demonstrate that diastolic performance in the failing heart correlates inversely with protein levels of NCX1 [17,20,59].
Chronic administration of KB-R7943 induces up-regulation of cardiac NCX1
2009, Journal of Biological Chemistry
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Please address all correspondence to: Dr Sian E. Harding, Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse StLondon SW3 6LY, UK. Tel: 0044 207 351 8146. Fax: 0044 207 823 3392. E-mail: [email protected]